Evidence is presented to substantiate and more precisely define the postulate that catecholamine neucoltransmitters may be released by a neuronal transport process distinct from exocytosis. This is a continuing investigation of a model synaptic system consisting of a calcium depending release of 3H-norepinephrine (3H-NE) from rat heart slices incubated in a Na ion deficient medium. It appears that a calcium dependent process directs norepinephrine loaded intraneuronal binding sites to a transport site on the plasma membrane. The 3H-NE appears to be passed directly from its binding site to the outward transport system. Amines therefore can be transported across an intact membrane without involving a process of exocytosis. Reserpine and Li ion appears to disrupt this process since they elicit a calcium independent release of deaminated metabolites. Studies now indicate that 3H-NE is transported directly from vesicles whose membrane form a new structure that retained the transport mechanism of both. Thus the release was inhibited by extracellular, energy-conserving, phosphorylated nucleotides. A Mg ions ATP dependent transport mechanism in the membrane of storage vesicles has been reported.